Effects of Sympathetic Vasoconstrictor Fibres, Noradrenaline and Vasopressin on the Intestinal Vascular Resistance during Constant Blood Flow or Blood Pressure

SUMMARY1. The effects of severe arterial hypoxia on the blood flow in the portal vein, and in kidney, muscle and skin beds have been determined in normal unanaesthetized rabbits, in animals without functioning autonomic effectors, and in rabbits with section of the carotid sinus and aortic nerves.2. The resting blood flows in the above regions were not significantly different in the three groups.3. The susceptibilities of the various beds to the local dilator effects of arterial hypoxia (assessed from the responses of animals without functioning autonomic effectors) were markedly different; vasodilatation was by far the greatest in the portal bed, followed in order by the renal, skin and muscle beds.4. Section of the carotid sinus and aortic nerves completely abolished reflex activity, and the pattern of peripheral blood flow changes was similar to that of animals without functioning autonomic effectors. The findings suggest that the arterial chemoreceptors are the primary afferent source of reflex control of the peripheral circulation in arterial hypoxia.5. In normal animals with intact reflexes there was sustained vasoconstriction throughout the treatment period in the portal and renal bed. The net vasomotor effects in muscle and limb skin were small owing to the operation of a number of factors, which opposed the effects of reflexly increased sympathetic nerve activity.

Section: Discussioncontrasting

confidence: 44%

Local and reflex factors affecting the distribution of the peripheral blood flow during arterial hypoxia in the rabbit

Chalmers

Korner²,

White³

1967

“…In both organs, escape occurs during constant flow perfusion and the initiating factor cannot be the decrease in total arterial flow (Dresel & Wallentin, 1966;Greenway et al 1967). However, as Dresel & Wallentin pointed out, these experiments did not exclude the possibility that a local accumulation of metabolites or the opening of shunt vessels results in a redistribution of the flow through certain areas of the organs.…”

Section: Introductionmentioning

confidence: 82%

Comparison of the effects of hepatic nerve stimulation on arterial flow, distribution of arterial and portal flows and blood content in the livers of anaesthetized cats and dogs

Greenway¹,

Oshiro²

1972

SUMMARY1. The responses to hepatic nerve stimulation were studied in cats and dogs anaesthetized with sodium pentobarbitone. In three series of experiments, hepatic arterial flow was recorded by an electromagnetic flowmeter, intrahepatic distributions of arterial and portal flows were studied by radioactive microspheres, and hepatic volume responses were measured by a plethysmographic method.2. In cats, nerve stimulation produced a frequency-dependent decrease in hepatic arterial flow which was not maintained and autoregulatory escape occurred. In dogs, the initial decrease in arterial flow was similar but escape did not occur and the vasoconstriction was well maintained.3. In both cats and dogs, stimulation of the hepatic nerves did not cause a redistribution of either arterial or portal flows within the liver. Autoregulatory escape in the liver of the cat was not associated with an intrahepatic redistribution of arterial flow and is best interpreted as relaxation of the same vessels which were initially constricted, due to increased production of a vasodilator factor.4. Stimulation of the hepatic nerves caused a marked frequencydependent decrease in hepatic volume which was well maintained and the responses were similar in cats and dogs. The quantitative importance of the liver as a blood reservoir is compared in relation to other vascular beds and the concept of the blood volume reserve is discussed.

“…However, the escape from vasoconstrictor fibre influence might also be ascribed to an autoregulatory phenomenon, perhaps on a myogenic or a. metabolic basis. The experiments in which polythene long-circuits were used confirm that such long-circuits introdiuce an unknown factor which can reduce the vascular response to nerve stimulation by as much as 50 %r (Dresel & Wallentin, 1966) and the results obtained must be treated with caution. However, these experiments suggest that the hepatic artery resistance vessels exhibit escape from the effects of stimulation of the: hepatic nerves as readily during constant flow perfusion as during constant, pressure perfusion.…”

Section: Pressure-flow Curves For the Hepatic Arterymentioning

confidence: 99%

“…However, these experiments suggest that the hepatic artery resistance vessels exhibit escape from the effects of stimulation of the: hepatic nerves as readily during constant flow perfusion as during constant, pressure perfusion. This means that, as in the intestine (Dresel & Wallentin, 1966), neurogenic reduction of the total artery flow cannot be the initiating factor.…”

Section: Pressure-flow Curves For the Hepatic Arterymentioning

confidence: 99%

The effects of stimulation of the hepatic nerves, infusions of noradrenaline and occlusion of the carotid arteries on liver blood flow in the anaesthetized cat

Greenway¹,

Lawson²,

Mellander³

1967

110

SUMMARY1. In anaesthetized cats, the hepatic artery, portal vein and inferior vena cava pressures and the hepatic artery and portal vein flows were recorded using pressure transducers and electro-magnetic flowmeters.2. The hepatic nerves were stimulated with maximal stimuli for periods of 2-5 min. The magnitude of the response varied with the frequency of stimulation over the range 1-10 impulses/sec. The resistance to flow increased in both the hepatic artery and the portal vein.3. In the hepatic artery, mean pressure remained virtually constant, while the flow showed an initial marked decrease followed by a return towards the control level. In the portal vein, the flow remained constant while portal pressure showed a maintained increase. These responses were unaffected by previous administration of atropine and propranolol, but were blocked by phenoxybenzamine.4. Infusions of noradrenaline into the hepatic artery produced changes similar to those following stimulation of the nerves. In contrast, when the hepatic arterial pressure was maintained constant, intravenous infusions of noradrenaline produced a maintained decrease in hepatic artery flow.5. The occurrence of autoregulation of the hepatic artery flow at arterial pressures above 80-100 mm Hg was confirmed.6. Occlusion of the carotid arteries caused a rise in arterial pressure with little change in hepatic artery flow, but when the hepatic artery pressure was maintained at the pre-occlusion level the flow showed an abrupt decrease, usually followed by a recovery towards the control level. This decrease was abolished by section of the hepatic nerves and removal of the adrenal glands.